Volume 14, No 5, Oct 2004

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 14 Issue 5, October 2004: 434-438

ORIGINAL ARTICLES

The effect of C-terminal fragment of JNK2 on the stability of p53 and cell proliferation

Zhi Min Yin^1,*, Jian SiMa¹, Yi Fan Wu¹, Jian Zhu¹, Yong Jiang²

¹Jiangsu Province Key Laboratory of Biochemistry and Molecular Biology, College of Life Science, Nanjing Normal University, Nanjing 210097, China
²Department of Pathophysiology and Key Lab for Shock and Microcirculation of PLA, The First Military Medical University, Guangzhou 510515, China Correspondence: Zhi Min YIN(Zhiminy_2000@yahoo.com)

The basal activity of JNK is low in normal growing cells and inactivated JNK targets p53 for ubiquitination. To elucidate if the C-terminal part of JNK is responsible for its binding to p53, the low background tet-off inducible NIH3T3 cell line was selected by luciferase reporter gene and a double stable C-JNK Aa (203-424) cell line was established. After withdrawing tetracycline, the C-JNK fragment expression was induced and cell growth was dramatically inhibited 24 h later. However, the expresion of p53 was found to be increased after the induction of C-JNK fragment, evaluated by transfecting p21waf-luciferase reporter genes. Our further studies showed that C-JNK fragment could form complex with p53 both in vivo and in vitro. Induction of C-JNK fragment in vivo can increase p53 stability by inhibiting p53 ubiquitination.

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